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| 1 | Mitophagy links oxidative stress conditions and neurodegenerative diseases显示文摘Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases. | Ulfuara Shefa Na Young Jeong In Ok Song Hyung-Joo Chung Dokyoung Kim Junyang Jung Youngbuhm Huh | 2019 | Neural Regeneration Research2019，14，5： | 21 |
| 2 | Temperature data from satellite imagery and the distribution of schistosomiasis in Egypt显示文摘 | Malone JB Huh OK Fehler DP | 1994 | Am J Trop Med Hyg1994，50，6： | 1 |
| 3 | Temperature data from satellite imagery and the distribution of schistosomiasis in Egypt显示文摘 | Malone JB Huh OK Dermis P | 1994 | Am J Trop Med Hyg1994，50，： | 1 |
| 4 | A global network for the control of snail-bome disease using satellite surveillance and geographic information systems显示文摘 | Malone Jb Bergquist Nr Huh Ok | 2001 | Acta Trop2001，79，1： | 1 |
| 5 | Temperature data from satellite imagery and the distribution of schistosomiasis in Egypt显示文摘 | Malone JB Huh OK Fehler DP | 1994 | AM J Trop Med Hyg1994，50，： | 1 |
| 6 | Anatomical distributional defects in mutant genes associated with dominant intermediate Charcot-Marie-Tooth disease type C in an adenovirus-mediated mouse model显示文摘Dominant intermediate Charcot-Marie-Tooth disease type C(DI-CMTC) is a dominantly inherited neuropathy that has been classified primarily based on motor conduction velocity tests but is now known to involve axonal and demyelination features.DI-CMTC is linked to tyrosyl-t RNA synthetase(YARS)-associated neuropathies,which are caused by E196 K and G41 R missense mutations and a single de novo deletion(153-156 del VKQV).It is well-established that these YARS mutations induce neuronal dysfunction,morphological symptoms involving axonal degeneration,and impaired motor performance.The present study is the first to describe a novel mouse model of YARS-mutation-induced neuropathy involving a neuron-specific promoter with a deleted mitochondrial targeting sequence that inhibits the expression of YARS protein in the mitochondria.An adenovirus vector system and in vivo techniques were utilized to express YARS fusion proteins with a Flag-tag in the spinal cord,peripheral axons,and dorsal root ganglia.Following transfection of YARS-expressing viruses,the distributions of wild-type(WT) YARS and E196 K mutant proteins were compared in all expressed regions; G41 R was not expressed.The proportion of Flag/green fluorescent protein(GFP) double-positive signaling in the E196 K mutant-type mice did not significantly differ from that of WT mice in dorsal root ganglion neurons.All adenovirus genes,and even the empty vector without the YARS gene,exhibited GFP-positive signaling in the ventral horn of the spinal cord because GFP in an adenovirus vector is driven by a cytomegalovirus promoter.The present study demonstrated that anatomical differences in tissue can lead to dissimilar expressions of YARS genes.Thus,use of this novel animal model will provide data regarding distributional defects between mutant and WT genes in neurons,the DICMTC phenotype,and potential treatment approaches for this disease. | Seo Jin Lee Sandesh Panthi Hyun Woo Jo Jaeyoung Cho Min-Sik Kim Na Young Jeong In Ok Song Junyang Jung Youngbuhm Huh | 2017 | Neural Regeneration Research2017，12，3： | 1 |
| 7 | Temperature data from satellite imagery and the distribution of schistosomiasis in Egypty显示文摘 | Malone JB Huh OK | 1994 | Am J Trop Med Hyg1994，50，6： | 1 |
| 8 | A global network for the control of snail-borne disease using satellite surveillance and geographic information systems显示文摘 | Malone JB Bergquist NR Huh OK | 2001 | Acta Trop2001，79，1： | 1 |
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